Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-8-22
pubmed:abstractText
Bradykinin is one of the key molecules involved in the disruption of the blood-brain barrier and blood-spinal cord barrier occurring after spinal cord injury (SCI). Previously we have shown a biphasic opening of the blood-spinal cord barrier as well as increased transport of tumor necrosis factor-alpha (TNFalpha) after SCI by compression of the lumbar spinal cord in mice. To evaluate the role of bradykinin in the two phases of blood-spinal cord barrier disruption, we pretreated mice with a potent bradykinin antagonist, the decapeptide B9430, before SCI. Our results show that B9430 decreased the general blood-spinal cord barrier disruption occurring immediately after SCI but failed to affect the delayed opening of the blood-spinal cord barrier observed 72 h after SCI. By contrast, the entry of TNFalpha after SCI was not affected by B9430 treatment. We conclude that bradykinin is involved in the early phase of blood-spinal cord barrier disruption, with B9430 non-selectively blocking this early disruption without affecting the selective transport system for TNFalpha. This indicates the therapeutic potential of bradykinin antagonists in ameliorating tissue damage induced by SCI.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0304-3940
pubmed:author
pubmed:issnType
Print
pubmed:day
6
pubmed:volume
307
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
25-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Bradykinin antagonist decreases early disruption of the blood-spinal cord barrier after spinal cord injury in mice.
pubmed:affiliation
VA Medical Center and Department of Medicine, Tulane University School of Medicine, 1601 Perdido Street, New Orleans, LA 70112, USA. wpan@tulane.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.